Transfer rates of pathogenic bacteria during pork processing.

We examined the rates of pathogenic bacterial cross-contamination from gloves to meat and from meat to gloves during pork processing under meat-handling scenarios in transfer rate experiments of inoculated pathogens. The inoculated pork contained ~5-6 Log10 CFU/g pathogenic bacteria like Escherichia coli (E. coli), Staphylococcus aureus (S. aureus), Listeria monocytogenes (L. monocytogenes), and Salmonella enterica subsp. enterica (Sal. enteritidis). On cotton gloves, after cutting the pork, the cutting board, knife, and cotton gloves showed 3.07-3.50, 3.29-3.92 and 4.48-4.86 Log10 CFU/g bacteria. However, when using polyethylene gloves, fewer bacteria (3.12-3.75, 3.20-3.33, and 3.07-3.97 Log10 CFU/g, respectively) were transferred. When four pathogens (6 Log10 CFU/g) were inoculated onto the gloves, polyethylene gloves showed a lower transition rate (cutting board 2.47-3.40, knife 2.01-3.98, and polyethylene glove 2.40-2.98 Log10 CFU/g) than cotton gloves. For cotton gloves, these values were 3.46-3.96, 3.37-4.06, and 3.55-4.00 Log10 CFU/g, respectively. Use of cotton gloves, polyethylene gloves, knives and cutting boards for up to 10 hours in a meat butchering environment has not exceeded HACCP regulations. However, after 10 h of use, 3.09, 3.27, and 2.94 Log10 CFU/g of plate count bacteria were detected on the cotton gloves, cutting board, and knives but polyethylene gloves showed no bacterial count. Our results reveal the transfer efficiency of pathogenic bacteria and that gloved hands may act as a transfer route of pathogenic bacteria between meat and hands. The best hand hygiene was achieved when wearing polyethylene gloves. Thus, use of polyethylene rather than cotton gloves reduces cross-contamination during meat processing.

Metformin prevents an adaptive increase in GSH and induces apoptosis under the conditions of GSH deficiency in H4IIE cells.

The antidiabetic effect of metformin is mediated by activation of AMP-activated kinase (AMPK). This study investigated whether metformin at a high pharmacologic concentration alters the levels of cellular GSH in H4IIE hepatocytes and if so, whether the agent affects cell viability under GSH-deficient conditions. Treatment of cells with either metformin or 5-aminoimidazole-4-carboxamide riboside (AICAR) increased dichlorofluorescein oxidation, as did tert-butylhydroxyquinone (t-BHQ). Metformin or AICAR treatment blocked a rebound increase in GSH produced by t-BHQ and decreased GSH content below that of control. Exposure of cells to metformin or metformin + t-BHQ for 24 hr did not produce cell death. However, metformin treatment in combination with t-BHQ for a prolonged period of time (48 hr) at the concentrations, at which each agent was non-toxic, produced apoptosis. Treatment of AICAR with t-BHQ resulted in similar effects. Induction of apoptosis by the combination treatment was evidenced by changes in mitochondrial cytochrome c content, BCl(xl) expression, poly(ADP-ribose)polymerase (PARP) cleavage and caspase-3 activation. Compound C, an AMPK inhibitor, reversed apoptosis and changes in the apoptotic markers, suggesting a role of AMPK activation by metformin in the apoptotic process. Similarly, metformin treatment, when combined with buthionine sulfoximine or doxorubicin, induced apoptosis. Our data indicated that metformin prevents an adaptive increase in cellular GSH in H4IIE cells, and therefore induces apoptosis under the conditions of GSH deficiency.